Vascular Flashcards

(102 cards)

1
Q

Aorta extends from?

A

aortic valve to proximal iliac bifurcation at L4

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2
Q

What are 3 segments of aorta?

A

Ascending aorta (from aortic valve to T4)

Descending Aorta (2 parts)
1. Thoracic Aortic (from aortic arch to diaphragm)
2. Abdominal Aorta (from below diaphragm until bifurcation into common iliac arteries)

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3
Q

Ascending Aorta begins, ends, features

A

Begins: At the aortic valve, located at the top of the left ventricle of the heart.

Ends: At the beginning of the aortic arch, around the level of the sternal angle (between the 2nd and 3rd rib).

Features: The ascending aorta gives rise to the coronary arteries, which supply blood to the heart.

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4
Q

Aortic Arch begins, ends, features

A

Begins: At the end of the ascending aorta.

Ends: Just after the origin of the three main arteries that branch from it

(brachiocephalic trunk, left common carotid artery, and left subclavian artery), at the level of the T4 vertebra.

Features: This portion curves over the heart and directs blood to the upper body.

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5
Q

Descending Thoracic Aorta begins, ends, features

A

Begins: Just after the aortic arch at the T4 vertebra.

Ends: As it passes through the diaphragm at the level of the T12 vertebra.

Features: The thoracic aorta supplies blood to the chest wall, lungs, and esophagus.

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6
Q

Abdominal aorta

A

Begins: At the aortic hiatus in the diaphragm (around the T12 level).

Ends: At the level of the L4 vertebra, where it bifurcates into the common iliac arteries.

Features: The abdominal aorta supplies blood to the abdominal and pelvic organs, as well as the lower limbs.

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7
Q

Bifurcation of the aorta

A

At the L4 vertebra, the abdominal aorta splits into the left and right common iliac arteries, which then continue to supply the lower limbs and pelvis.

5 major branches:
Celiac trunk
Superior mesenteric artery
Left & Right renal arteries
Inferior mesenteric artery

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8
Q

Nerves of aorta is primarily innervated by?

A

Autonomic Nervous System (ANS)

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9
Q

What are the nerve plexuses related to aorta?

A

Celiac plexus
Superior mesenteric
Inferior mesenteric

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10
Q

What is the artery of ADAMKIEWICZ?

A

blood vessels supplies most oxygenated blood to spinal cord.

Originate: between T8-T12 vertebrae
(though it can arises anywhere from T5 to L3)

Largest radiculomedullary artery (meaning it provides arterial blood to the spinal cord)

supplying the lower two-thirds of the spinal cord.

Adamkiewicz supply blood flow to Anterior Spinal Artery (Which supplies anterior 2/3 of spinal cord).

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11
Q

Anterior 2/3 of spinal cord is supplied by? and responsible for?

A

anterior two-thirds of the spinal cord is supplied by anterior spinal artery. Anterior spinal artery is supplied by Adamkiewicz from T8-T12

This region is responsible for motor function and sensation, so damage or blockage can lead to severe motor deficits or paralysis.

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12
Q

Injury to Adamkiewicz artery can result in?

A

surgical complications, trauma, or vascular disease—can lead to spinal cord ischemia/spinal cord infarction, resulting in paraplegia or other serious neurological deficits.

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13
Q

Which surgery is at risk for injured Adamkiewicz surgery?

A

Thoracolumbar region.

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14
Q

What is Atherosclerosis?

A

plague, fat, cholesterol builds up on walls of arteries.

Plagues harden > narrow and stiffness of arteries > limit blood flow

If occurs in peripheral arteries (outside of heart and brain) > PVD

PVD primarily affects arteries in the legs but can also impact arteries in the arms and organs. Reduced blood flow due to atherosclerosis can result in pain, especially during physical activity, and, in severe cases, can cause tissue damage and gangrene.

Atherosclerosis is systemic and progressive

Primarily affects the arteries due to plaque formation which leads to stenosis and potential occlusion of the lumen

Atheromatous plaques form and reduce distal blood flow

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15
Q

Plaque Formation in Atherosclerosis

A

look at the word doc

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16
Q

RF for atherosclerosis?

A

Advanced Age
Smoking
HTN
DM
Insulin resistance
Obesity
Family hx/genetic predisposition
Physical inactivity
Gender (M>F)
Hyper/hypomocysteinemia (High or low levels of total homocysteine in blood – B6, 9, 12)
Elevated C-reactive protein, elevated lipoprotein
Hyperglyceridemia, hyperlipidemia
Renal disease

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17
Q

Most common LowerExtremity vessels affected by Atherosclerosis

A

Superficial femoral artery
Popliteal artery

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18
Q

How to treat Atherosclerosis-medication? ?

A

First line: Statins > lower cholesterols and stabilize plagues

  1. Antiplatelet (baby aspirin > prevent clots by prevent platelet aggregation > reduce risk of stroke or heart attack)
  2. Anti-HTN (ACEin, ARBs, Betablocker, CCB)
  3. Blood sugar control. prevent further plaque build up
  4. Anti-inflammatory medications
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19
Q

**Betablockers in atherosclerosis for HTN

A

Used for patients with PVD that are high-risk for myocardial ischemia and infarction

AAA repair – 10-fold decrease in cardiac morbidity with adequate Beta blockade

Helps with myocardial oxygen supply and demand

Target heart rate is 50-60bpm

Should be started days to weeks before surgery for best results

Perioperative Beta blocker started within 1-day or less before non cardiac surgery prevents nonfatal MIs but increases hypotension, stroke, bradycardia and death (BB prevents MIs but can cause hypotension and brady)

Atenolol, Metoprolol, labetalol, propanolol

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20
Q

Should you give Aspirin pre-op?

A

NO (stop 7 days)
restart 2-8 days after surgery

giving ASA can increase risk of bleeding

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21
Q

What counts for more than 1/2 the mortality associated with PVD?

A

Adverse cardiac events
> know pt cardiac function pre-op for vascular pt

Association b/w PVD and CAD

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22
Q

Diabetes put pt at risk for what?

A

Higher risk of MI and wound infection

Hyperglycemia can exacerbate neurologic injury: tight control for CEA (carotid endarterectomy & thoracic aortic procedures

Must check glucose pre-op for vascular pt

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23
Q

If a pt on chronic dialysis, must make sure that?

A

they have dialysis the DAY before
or Same day of surgery (prior to sx)

check baseline BUN and Creatine

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24
Q

Aortic surgery increase risk for what?

A

due to the level of aortic clamping > postop kidney dysfunction is common

Biggest issues: Suprarenal at highest risk- decreases renal blood flow by 80%

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25
Carotid Artery Disease also known as?
Carotid Artery Stenosis
26
Symptomatic Carotid Artery Stenosis
Patients with transient ischemic attack (TIA) or mild stroke who have 70-99% stenosis in the carotid artery. Some cases with 50-69% stenosis, if there are high stroke risk factors.
27
When is Carotid Endarterectomy is recommended?
CEA is usually recommended within two weeks of a TIA or minor stroke to prevent further events.
28
Indication of CAE
Asymptomatic Carotid Artery Stenosis: CEA may be considered in patients with 60-99% stenosis even without symptoms, especially in those under 75 years old and in good health. The decision is influenced by the patient's overall health, life expectancy, and the skill and experience of the surgical team.
29
what are the S/S of Carotid Disaese?
Usually caused by embolization Manifests as amaurosis fugax, paresthesia, clumsiness of extremities, speech problems Carotid duplex ultrasonography > Duplex ultrasound is the primary noninvasive diagnostic tool for detecting, grading and monitoring of carotid artery stenosis due to its low cost, high resolution, and widespread availability. Sensitivity & specificity to detect stenosis >60% - approximately 94%
30
amaurosis fugax is
painless loss of vision in 1 eyes refers to a transient monocular visual loss, is considered a medical emergency. Usually caused by atherosclerotic emboli that leads to retinal artery occlusion, or other conditions, such as inflammation of the associated nerves and arteries
31
what is angiogram?
imaging test uses X rays visualize carotid arteries inject contrast dye into groin or arm catheter take images ==> identify stenosis (narrowing), blockages.
32
Head and neck region obtain most of its blood supply via?
Carotid and vertebral arteries
33
Carotid arteries mainly supply
brain and face
34
Right Common Carotid Artery originates in and from
in the neck and from the brachiocephalic artery
35
Left Common Carotid Artery Arises
in the thorax from the arch of the aorta
36
Both R and L common carotid arteries bifurcate in the _____ at the level of _____
bifurcate: in the NECK at the level of: CAROTID SINUS
37
Both R and L common carotid artery after bifurcation > branches into?
into the internal carotid artery (ICA), which supplies the brain the external carotid artery (ECA), which supplies the neck and face
38
At which level does carotid arteries bifurcate into ECA and ICA
Carotid sinus or the upper border of the thyroid cartilage (typically at the level of the fourth or fifth cervical vertebra)
39
Why is the bifurcation point of carotid arteries significant?
serves as a point for the location of the "carotid body," a chemoreceptor and the "carotid sinus," a baroreceptor. CHEMORECEPTOR = CAROTID BODY BARORECEPTOR = CAROTID SINUS
40
What is Carotid body chemoreceptor?
is sensitive to: decreased PO2 increased PCO2 decreased pH of blood ==> responsible for alerting the brain to change the respiratory rate.
41
What is carotid sinus baroreceptors
respond to changes in the stretch of the blood vessel and are responsible for detecting changes and maintaining blood pressure. (bezold Jerish reflex)
42
Bezold Jerish Reflex
Main effects: Bradycardia, hypotension, and coronary vasodilation Trigger: Decreased preload (less venous return → underfilled left ventricle) Mechanism: Receptors in the left ventricle (both chemo- and mechanoreceptors) sense poorly filled or contracting ventricle This activates the Bezold–Jarisch reflex Leads to inhibition of the sympathetic nervous system (SNS) and activation of the parasympathetic nervous system (PSNS) Result: → Bradycardia, hypotension, and coronary artery dilation
43
What is Carotid Sinus
a small dilated area located at the bifurcation of the common carotid artery, where it splits into the internal and external carotid arteries. It contains baroreceptors, which are specialized sensors that detect changes in blood pressure.
44
How does Carotid Sinus (Baroreceptor detect changes?)
1. The baroreceptors in the carotid sinus are sensitive to the stretch of the arterial wall, which corresponds to blood pressure. 2. When blood pressure increases, these receptors are stretched more, sending signals to the brain (specifically, the medulla oblongata) via the glossopharyngeal nerve (cranial nerve IX). ==> Reduces Sympathetic Nervous System activity and increase PSNS. Slow HR, dilates blood vessles, decrease BP 3. When blood pressure drops, the signals from these receptors decrease. Causes SNS acitivty increase > vasoconstriction > increase HR and BP
45
What is cerebral autoregulation?
Cerebral autoregulation is the brain's intrinsic ability to maintain stable blood flow across a range of blood pressures, protecting the brain from ischemia or hyperperfusion. The brain's blood vessels can constrict or dilate in response to changes in systemic blood pressure. when blood pressure increases, cerebral vessels constrict to reduce blood flow. When blood pressure decreases, vessels dilate to increase blood flow.
46
How is CBF maintain relatively constant at different CPP
because of cerebrovascular autoregulation
47
Brain CBF autoregulation is maintained when MAP range is?
60-150
48
CPP formula?
CPP = MAP-ICP (or CVP, which ever is higher)
49
Chronic HTN shifts autoregulatory curve to the??
RIGHT require a higher MAP
50
if brain autoregulation is impaired, what happened?
In patients with conditions like hypertension, diabetes, or atherosclerosis, the range and effectiveness of autoregulation may be reduced. These patients may have a narrower range of MAP within which their brain can effectively autoregulate. During surgeries like CEA, cerebral autoregulation may be temporarily disrupted, making patients more vulnerable to ischemic events or hyperperfusion injury if blood pressure is not carefully controlled.
51
**The carotid sinus plays a central role in ___
sensing and regulating blood pressure through baroreceptors. High BP → increased stretch → increased baroreceptor firing → activates parasympathetic system → ↓ HR, ↓ contractility, ↓ BP Low BP → decreased stretch → decreased baroreceptor firing → activates sympathetic system → ↑ HR, ↑ contractility, ↑ vasoconstriction, ↑ BP
52
**During CEA manipulation of the carotid sinus can lead to
transient or lasting baroreceptor dysfunction, resulting in labile blood pressure.
53
Cerebral autoregulation maintains consistent blood flow to the brain over a range of pressures but may be compromised in which surgery procedure?
CEA necessitating meticulous blood pressure management to protect brain health.
54
Anesthetic GOALS for CEA?
Protection of heart and brain from ischemic injury Control HR and arterial blood pressure Ask surgeon acceptable BP range Know preop BP Ablate surgical pain and stress responses *** have an awake patient at the conclusion of surgery for immediate neurological examination!
55
After surgery, patient must be awake for what?
neurological examination
56
How to prepare for CEA? supplies
ECG monitors II, V5 Watch for ST segment changes Radial Arterial Line NIBP contra lateral arm Two large bore peripheral IVs Stopcocks placed close to patient port for medication gtts IVAC pumps Eye protection
57
What medications to prep for CEA?
Propofol - induction Fentanyl – small amts Etomidate - induction NDMR Beta blocker (esmolol) Vasopressors Inhaled volatile agents Remifentanil; dexmedetomidine ACT machine/LR cuvettes in OR
58
During Cross clamping of CEA
must maintain Arterial Blood Pressure 10% ABOVE baseline
59
Head foams or Pillows for this procedure? CEA
Head foams NO PILLOWS
60
What are the UPPERs for CEA?
Phenylephrine, norepinephrine ephedrine (supply and demand mismatch; know your drugs
61
What are the DOWNERS for CEA?
BP nitroglycerin, Nipride, Nicardipine
62
What can happen during surgical manipulation of CEA?
Surgical manipulation of carotid sinus with activation of baroreceptor reflexes Causes abrupt bradycardia and hypotension
63
How to blunt the baroreceptor reflects of carotid sinus upon surgical stimulation during CEA?
Stop surgical manipulation Infiltrate carotid bifurcation w 1% lidocaine This can help blunt reflex
64
Stump pressure
Stump Pressure is the pressure measured in the internal carotid artery (ICA) distal to the surgical clamp during carotid endarterectomy (CEA). reflects how well blood can reach the brain through collateral circulation (mainly via the Circle of Willis) while the carotid artery is clamped. to assess collateral flow and need for shunt (controversial) Stump pressure < 40-50 mm Hg reflects hypoperfusion (low collateral flow) ==> Criteria for shunt placement Goal of SHUNT: + maintain CBF, decrease cerebral ischemia + Increase collateral flow with use of shunt + Decrease cerebral metabolic requirements
65
What to AVOID during CLAMPING?
Avoid hypotension during cross clamp Avoid hypercapnia (goal 32-35) can cause "steal” phenomenon High PaCO₂ → cerebral vasodilation in normal brain regions → “steal phenomenon” (blood is diverted away from ischemic areas that cannot dilate). Avoid hyperglycemia – brain swelling. LR vs NS (avoid LR bc it contains Lactate which can convert to glucose) Hypothermia (Most avoid Bair Huggers) Pharmacologic choices
66
Why MUST AVOID Hypercapnea during CEA?
Hypercapnia can significantly impact cerebral circulation during CEA. CO₂ is a potent cerebral vasodilator > increasing CBF. However, hypercapnia can also lead to uneven blood distribution, worsening ischemic conditions in vulnerable brain areas. (Steal phenomenon) increased ICP: Higher CO₂ levels can elevate ICP, particularly in patients with limited cerebral autoregulation, increasing the risk of cerebral edema and compromised perfusion. Enhanced steal phenomenon: Hypercapnia can exacerbate the steal phenomenon, which can shunt blood away from already ischemic areas (in the case of CEA, from the brain region served by the narrowed carotid artery).
67
Cerebral Monitors for CEA
Awake Patient - Gold Standard EEG - High false-positives SSEPs - Indicates subcortical ischemia Stump Pressure - Poor sensitivity/specificity Transcranial Doppler - Assess hemodynamic ischemia, shunt function, embolic phenomenon, reperfusion syndrome
68
What is Cerebral oximetry
Determine cerebral saturation > infared light > absorption of this light by Oxygenated and deoxygenated Hgb determine overal Sat.
69
Why HEPARIN is used during CEA?
prevent thromboembolic complications 10,000u drawn up – surgeon will order dose (100u/kg) Check Blood ACT prior to giving heparin and 3-5 minutes after initial dose; then q20-30 minutes (use LR cuvettes) Prior to internal carotid artery clamping What level? must achieve 250s – 375s ==> Protamine is used to reverse heparin
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Before carotid artery clamping, ACT must achiieve what level?
250s – 375s
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what to know about a shunt during CEA
Surgeon decides if the patient needs a shunt during the procedure – this is something I ask during time – out Know the extent of the carotid disease in the ipsilateral carotid artery Shunts are most often utilized with severe bilateral carotid disease Inserting the Shunt: After clamping the artery, the surgeon makes a small incision in the carotid artery and inserts a flexible tube (shunt) that diverts blood around the surgical site. The shunt typically extends from one end of the clamped artery section to the other, creating a temporary blood flow channel. Removing the Shunt: Once the plaque is removed and the artery is closed, the shunt is removed before blood flow is restored.
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Emergence in CEA and extubation
Awake Intubation with minimal coughing Resident will hold pressure on neck to avoid straining Precedex is a great emergence drug – not too much Neuro exam immediately after extubation Full reversal Avoid too much versed Surgeon/Resident will do neuro exam – stick out tongue, shrug shoulders, smile, squeeze hands – each correlate to a specific cranial nerve Turn inhalational agent off early
73
CEA with Regional Anesthesia is it possible?
Gold standard Superficial cervical plexus block: C2-C4 dermatomes Block in preop to assure completion Extensive patient preparation – must be able to lie still – warn them about drapes, pressure, talking, count to 10, state name, constant communication w patient Caution with sedation – want to assess for stroke at all times – how?
74
***Which block is used for CEA?
Superficial Cervical Plexus Block C2-C4
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Why regional anesthesia is good for CEA?
Greater stability of BP Easy cerebral monitoring Avoid intubation Avoid negative inotropic agents Fewer episodes of EEG ischemia Reduced costs
76
Why regional anesthesia is bad for CEA
Patient panics Sudden loss of consciousness Onset of seizures Control of airway may be difficult Quality & timing of block
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***Post-op management of CEA
Assess for: Onset of new neurologic dysfunction Hemodynamic instability Respiratory insufficiency Cranial nerve deficits Hematoma Hyperperfusion syndrome
78
What is Hyper-perfusion syndrome?
a rare but serious complication that can occur after CEA. It typically occurs within days to weeks following surgery. Cause: During CEA, the restored blood flow can lead to a sudden increase in blood pressure and blood flow in the brain, especially in areas that were previously under-perfused. If blood flow regulation is disrupted, it can lead to hyperperfusion syndrome. Symptoms: Symptoms often include severe headache, nausea, vomiting, confusion, visual disturbances, and, in severe cases, seizures or intracerebral hemorrhage (bleeding in the brain). ==> These symptoms can resemble a stroke Risk Factors: high blood pressure after surgery, older age, poorly controlled preoperative hypertension, and previous history of stroke or transient ischemic attack (TIA). Management and Prevention: Close monitoring of blood pressure is crucial postoperatively, as controlling blood pressure can help reduce the risk.
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***What are common CRANIAL NERVE injuries post-CEA and DIAGNOSIS via NEURO EXAM?
Facial Nerve (CN VII) Injury: Diagnosed by asymmetric facial movements during voluntary actions like smiling or showing teeth. Glossopharyngeal Nerve (CN IX) Injury: Identified by impaired swallowing and reduced gag reflex on one side. Vagus Nerve (CN X) Injury: Diagnosed by hoarseness, uvula deviation, and diminished palatal elevation. Spinal Accessory Nerve (CN XI) Injury: Suspected if there is unilateral shoulder droop or weakness in head rotation against resistance. Hypoglossal Nerve (CN XII) Injury: Detected by tongue deviation toward the affected side and reduced lateral tongue movement.
80
2 most popular Aortic Disease?
aortic aneurysm aortic dissection
81
what is aortic aneurysm
abnormal bulging or dilation in a weakened part of the aorta. It can occur in the chest (thoracic aortic aneurysm) or abdomen (abdominal aortic aneurysm). If it ruptures, it can lead to severe internal bleeding.
82
What is aortic dissection
A tear in the inner layer of the aorta’s wall, allowing blood to flow between the layers of the wall and forcing them apart. This can cause severe pain and lead to life-threatening complications if untreated.
83
Symptoms of aortic aneurysm
75% asymptomatic Discovered by palpation of abdomen during physical exam X-ray, CT, or MRI for other conditions Pain in abdomen, chest, lower back, or groin can be indicative of impending rupture Acute pain - ruptured?
84
Risk factor for aortic aneurysm
Age: Risk increases significantly after the age of 65. Gender: Men are more prone to aneurysms than women. Family History: A family history of aneurysms can increase risk. Smoking: Smoking damages blood vessels, and smokers have a significantly higher risk of developing aneurysms, especially abdominal ones. High Blood Pressure (Hypertension): High blood pressure increases the stress on blood vessel walls, which can weaken them over time. Atherosclerosis (Hardening of the Arteries): Plaque buildup in the arteries can weaken the aortic wall. Genetic Disorders: Certain inherited conditions, like Marfan syndrome or Ehlers-Danlos syndrome, can weaken blood vessel walls and predispose individuals to aneurysms. Infections or Inflammation: Rarely, infections or inflammatory conditions can cause or worsen aneurysms.
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**Risk of rupture of aortic aneurysm is directly related to?
the luminal diameter of aneurysm
86
what is abdominal aortic aneurysm (AAA)
dilatation of abdominal aorta BELOW the level of the renal arteries
87
When is the risk of rupture increased in Aortic aneurysm
once aneurysm is >4.5-5 cm in diameter Increases by a median of 0.3 cm per year
88
How does law of Laplace related to the aortic aneurysm?
Law of Laplace the theoretical basis for using the “maximum diameter criterion” for AAA rupture potential prediction. This “law” states that the stress in the AAA wall is proportional to its diameter.
89
monitors requirements for open aortic surgery?
5 Lead ECG (II, V) 2 large bore PIV (RIJ) – blood tubing A-line (dominant arm) Central Access/SG ACT TEE or PVV Fluid Warmers 500cc pressure bags Cell Saver NGT Avoid HTN on induction (esmolol)
90
What is the approach for OPEN AORTIC SURGERY?
Approach Vertical anterior midline*** Retroperitoneal
91
Anesthesia goals for open aortic surgery?
Anesthetic technique - GA Tips: Keep the patient warm Keep HR slow (avoid Tachy) Avoid anemia (HCT>25-30) Prevent HTN EBL can be large
92
Which induction drugs for OPEN AAA patient?
Induction Agents: Typically, etomidate or propofol are used. Etomidate is preferred if the patient has a high risk of hemodynamic instability, as it has minimal impact on cardiovascular stability. Propofol can be used but requires careful titration due to its potential to cause hypotension. Opioids: Fentanyl or remifentanil are used to blunt sympathetic response, with remifentanil offering precise control due to its rapid onset and offset. Muscle Relaxants: Rocuronium may be preferred for intubation. Avoid long intubation technique.
93
Induction for open AAA notes
Avoid Hypotension and Hypertension: Both extremes should be prevented. Hypotension can compromise perfusion to vital organs, particularly the kidneys and spinal cord, while hypertension could stress the aneurysm, risking rupture. Avoid Tachycardia: Increased heart rate adds to myocardial oxygen consumption and places more pressure on the aneurysm. Beta-blockers (esmolol or metoprolol) may be given if heart rate control is needed. Gentle Induction: Slow, controlled induction is crucial to avoid sudden hemodynamic changes. Avoid Nitrous Oxide (N2O): Nitrous oxide can increase the risk of bowel distension, which may further complicate intra-abdominal conditions.
94
during PRE-CROSS CLAMPING PHASE of OPEN AAA, must prepare which drugs?
Vasoactive Drugs: Prepare for possible blood pressure increases by having vasodilators on hand, such as nitroglycerin or nicardipine, which can be titrated as needed.
95
during PRE-CROSS CLAMPING PHASE of OPEN AAA, must do WHAT?
Hemodynamic Optimization: Maintain baseline hemodynamics with adequate preload and stable cardiac output. Often a fluid bolus is administered before clamping to compensate for the sudden drop in venous return. Vasoactive Drugs: Prepare for possible blood pressure increases by having vasodilators on hand, such as nitroglycerin or nicardipine, which can be titrated as needed. Communication: Coordinate with the surgical team to know the exact timing of cross-clamping. Consider increasing inhalation agent or NTG bolus just prior to cross clamping Make sure you are heparinized – check ACT Fluid management is slightly hypovolemic May give mannitol 0.5g.kg 30 minutes prior to clamping
96
which AAA clamp place carries lowest risk for spinal cord injury?
infrarenal clamp
97
what is the effects of AORTIC CROSS CLAMP?*****
ABOVE the cross lamp: HYPERTENSION BELOW the cross clamp: Hypotension (80% reduction in MAP) Increases in afterload SVR MAP PAOP above the clamp PA Occlusion Pressure) CO usually decreases depending on LV function Increased cardiac oxygen consumption May experience redistribution of blood volume
98
What to do during clamping time?
Increase IVFs, Blood, CS slowly until closre to unclamping time. Clamp last 30-45 mins use short acting drugs Monitor urine output q30mins Ensure 1mL/kg/hr Avoid Hypovolemia, there will be large third space loss Crystalloid and blood management: cell saver and PRBC expect 600-2000 ml EBL Temperature control ACT monitoring; adjust Heparin dosing
99
Prior to Release of the Aortic Cross-Clamp (unclamping); must do what?
Preparation for Hypotension: Anticipate and prepare for a sudden drop in blood pressure upon unclamping, as blood rushes to previously ischemic areas. Volume Loading: Give fluid boluses and optimize preload prior to unclamping to maintain systemic pressure. Calcium Administration: Consider administering calcium to counteract myocardial depression associated with reperfusion. Vasopressors on Hand: Prepare vasopressors (e.g., phenylephrine, norepinephrine) to treat severe hypotension if it occurs upon release of the clamp. Communicate with the Surgeon: The timing of the clamp release should be carefully coordinated with the surgical team to ensure readiness for hemodynamic instability. Volume load including PRBCs – call perfusion for Cardiac surgery if available prior to removing cross clamp Decrease anesthetic agent and vasodilators Anticipation rapid volume infusion – 500cc bags Know hemodynamic profile Have a specific plan Then have a 2nd and 3rd plan May unclamp all at once or one leg at a time (more common)
100
Post-release of Aortic Cross Clamp
Monitor for Hypotension: Upon clamp release, be prepared to treat hypotension with vasopressors and fluid boluses. Reperfusion syndrome can lead to metabolic acidosis, hypocalcemia, and release of vasoactive substances, contributing to hypotension. Manage Acidosis and Hyperkalemia: Treat any metabolic acidosis or hyperkalemia that may occur due to the washout of ischemic metabolites. Assess Hemodynamic Status: Ensure that the patient is stable, with adequate perfusion to all organs. Optimize cardiac output and SVR to support post-clamp release circulation.
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